Evidence map›Paper›PMID 26625314›Full record

ArticleOncotarget2016

Critical role of PPARγ in myeloid-derived suppressor cell-stimulated cancer cell proliferation and metastasis.

Ting Zhao, Hong Du, Janice S Blum, Cong Yan

Open access · diamondAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.1field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

35 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
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  6. Recent insights into lysosomal acid lipase deficiency.Trends in molecular medicine · 2023
    Review
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  13. Nuclear Receptors and Lipid Sensing.Advances in experimental medicine and biology · 2022
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Ting ZhaoDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Hong DuDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Janice S BlumDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Cong YanDepartment of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Indiana University School of MedicineIndiana University – Purdue University Indianapolis · US

Funding

NCI NIH HHS CA138759NCI NIH HHS CA152099NCI NIH HHS R01 CA138759NCI NIH HHS R01 CA152099NHLBI NIH HHS HL087001NHLBI NIH HHS R01 HL087001NIAID NIH HHS R01 AI079065
6 · The paper itself

Abstract

Lysosomal acid lipase (LAL) is a key enzyme controlling neutral lipid metabolic signaling in myeloid-derived suppressor cells (MDSCs). MDSCs from LAL-deficient (lal-/-) mice directly stimulate cancer cell proliferation. PPARγ ligand treatment inhibited lal-/- MDSCs stimulation of tumor cell growth and metastasis in vivo, and tumor cell proliferation and migration in vitro. In addition, PPARγ ligand treatment impaired lal-/- MDSCs transendothelial migration, and differentiation from lineage-negative cells. The corrective effects of PPARγ ligand on lal-/- MDSCs functions were mediated by regulating the mammalian target of rapamycin (mTOR) pathway, and subsequently blocking MDSCs ROS overproduction. Furthermore, in the myeloid-specific dominant-negative PPARγ (dnPPARγ) overexpression bitransgenic mouse model, tumor growth and metastasis were enhanced, and MDSCs from these mice stimulated tumor cell proliferation and migration. MDSCs with dnPPARγ overexpression showed increased transendothelial migration, overactivation of the mTOR pathway, and ROS overproduction. These results indicate that PPARγ plays a critical role in neutral lipid metabolic signaling controlled by LAL, which provides a mechanistic basis for clinically targeting MDSCs to reduce the risk of cancer proliferation, growth and metastasis.

Indexed as

Cell CommunicationCell MovementCell ProliferationAnimalsAntigens, LyCarcinoma, Lewis LungCell DifferentiationCell Line, TumorCoculture TechniquesGenetic Predisposition to DiseaseLinoleic Acids, ConjugatedMelanoma, ExperimentalMembrane Potential, MitochondrialMice, Inbred C57BLMice, KnockoutMyeloid Cells9-hydroxy-10,12-octadecadienoic acidAntigens, LyLinoleic Acids, ConjugatedLy6G antigen, mouselysosomal acid lipase, mousemTOR protein, mousePPAR gammaReactive Oxygen SpeciesSterol EsteraseTOR Serine-Threonine Kinaseslipid metabolic signalinglysosomal acid lipasemyeloid-derived suppressor cellsperoxisome proliferator-activated receptor-γtumor growth and metastasis

Identifiers

PMID26625314
PMCPMC4811478
OpenAlexW2176078765

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.